Professor John Herman Taylor is at the very forefront of research into Crohn's disease and is a researcher at St Georges university London.
His vaccine is ready to go to human trials!

"We have made such a vaccine against MAP. It took us 8 years and cost, in cash terms, around £750,000. In extensive pre-clinical tests in mice and recently in cattle, the vaccine given in 2 shots has proved to be a powerful and safe long-lasting stimulant of anti-MAP immune cells with no side effects. It is highly effective against MAP. The vaccine has an excellent chance of doing the same thing for people with Crohn’s disease. With the funding we can get the vaccine GMP manufactured for human use and conduct the essential approved Clinical Trials."

I recently emailed the professor asking how things were going, he replied with this;

"The vaccine has given us excellent results in a 3 year BBSRC funded trial which finished this spring 2013.
No side effects.
We have just submitted a big grant application to the gov's Technology Strategy Board for money to manufacture the vaccine for human trials. Will hear Jan 24th whether we get final interview Feb 18/19.

Thanks....John H-T."

Administrator note: If you want to help open the attachment below. - Jennifer

Professor John Hermon-Taylor of Saint George's, University of London, is appealing for help to fund the final stages of development of a new Crohn's vaccine, which is now ready to proceed to human clinical trials.

Crohn's Disease
Crohn's disease is a severe inflammation of the intestine causing untold misery to almost 180,000 sufferers in the UK alone, and millions in the rest of the world. In many cases there are clear genetic links, but there is now good scientific evidence that the disease is caused by the bug Mycobacterium avium subspecies paratuberculosis (MAP).
Over a period of 8 years and at a cost of about £1.5 million, a research team at St George's Hospital Medical School (now St George's, University of London) led by Professor John Hermon-Taylor, has developed a state-of-the-art modern therapeutic vaccine to kill MAP and get rid of the distressing symptoms that blight the lives of so many sufferers and their families.

The vaccine will move to clinical trials and market development over the next three years. Over this period there is an absolute scientific requirement to develop tests that will establish proof that the vaccine will make people with Crohn's disease better. This final essential piece of scientific research will require £550,000.

You can also help by signing the online petition to the government for funding.

More about the disease, the new vaccine and the appeal...
What is Crohn's disease?
Most people know of someone with Crohn's disease symptoms. The principal manifestation is chronic inflammation of the intestine (colitis or IBD) with stomach pain and diarrhoea. Crohn's Disease (CD) affects your whole life, and that of your family. It is a 'new' disease which emerged in the mid 1940s and has now become common. There are probably more than 180,000 people suffering from it in Britain, rising at the rate of about 5,000 per year. In Europe CD is rising at about 25% per decade. In children the rate of increase is much higher.
Some Crohn's advice can be found on the Action Medical Research website.

What causes Crohn's disease?
The causation of Crohn's Disease has not been fully understood, nor recognised. As a consequence, conventional research and treatment are directed almost exclusively at suppressing the inflammation. This may help in the short term, but the disease almost invariably comes back. Most people with CD eventually have surgery, sometimes on more than one occasion. Epidemiological research has shown that the long term prospects for people with Crohns Disease have not improved significantly in 35 years.

Progress so far
Research we began and have continued since 1985, and which is now increasingly being taken up and confirmed by other research laboratories, shows that Crohn's Disease is largely caused by a bug called MAP (short for Mycobacterium avium subspecies paratuberculosis). The reliable scientific evidence for this has grown very strong.

• MAP infection is widespread in the animal world.
• MAP is being transmitted to humans in milk and from exposure to environmental sources like contaminated waters.
• MAP in people is difficult to detect. The tests have to be done just right. When they are, almost everyone with Crohn's Disease is found to be infected with MAP.
• MAP is what is called in microbiology a multi-host pathogen with the proven scientific ability to cause chronic inflammation of the intestine in many animals including primates. MAP is doing the same thing to people.

Modern Vaccines
MAP infections are difficult to eradicate. They are resistant to most antibiotics and drugs used to treat TB. In 1992, Prof Hermon-Taylor introduced a new treatment for Crohn's Disease using a combination of two recently available drugs more active against MAP, called rifabutin and clarithromycin. They work in over 50% of people with active CD who can take them. Relapses sometimes occur. New anti-MAP treatments such as modern therapeutic vaccines are needed. Conventional vaccines make antibodies to prevent disease. They could not work in CD as the MAP bugs are already there inside cells. Modern vaccines make armies of hunter-killer cells which patrol the body getting rid of infected cells. So modern vaccines can be used to treat diseases caused by chronic infections.

A Crohn's cure?
Prof Hermon-Taylor and his team began seeking funding in 2001. Since then they have received and committed over £1.5 million. With this they have designed and delivered a state-of-the-art modern anti-MAP vaccine. It consists of a critically important cassette of MAP DNA in two harmless carrier viruses called Ad5 and MVA. These carriers are already working in approved clinical trials with other modern vaccines. In the Crohn's Disease vaccination treatment procedure, the Ad5 is given first and the MVA boost 6 weeks later. In multiple tests over the last two years, the Crohn's vaccine has consistently proved to be effective both in treating existing MAP infection and protecting against subsequent MAP infection, without any side effects.

What is still needed?
We have come a long way and are nearly there. The Crohn's treatment will move to clinical trials and market development over the next 3 years. Over this period there is an absolute scientific requirement to develop new quantitative tests for MAP in humans, new immunological tests for MAP in humans, and tests for the specific immune responses of people to the vaccine. Together these tests will establish proof of concept that anti-MAP vaccination can make people with Crohn's disease better, and it does so by depleting or eradicating the MAP infection. This final essential piece of scientific research will require £550,000.

Why can't I find any decent information about this guy on google? He's mentioned once or twice in other peoples biographies on the St Georges website and theres that daily mail article but other than that it's just a load of extremely dated looking websites.

And OP where has your information come from?

EDIT:

I found a Facebook fundraising group run by his daughter, I can't link it as its against forum rules but I found the following post interesting.

A post on 4 Dec 2013:

"What's one thing you wish everyone knew about IBD?

That a treatment #vaccine for Crohn's has been made and is awaiting a trial in humans.
A Crohn's cure is so very close
Help me raise the money to fund the trial!"

I just finished watching those videos too. Aside from everything else, the bit that stood out to me the most was when he was talking about it being airborne (in either the 2nd or third part, Ican't remember) and people breathing it in and developing a cough before they developed Crohn's. That's exactly what happened to me. I had this horrible persistent cough for a couple of weeks before my Crohn's symptoms started showing up. Until that video I never would have thoughts the two would be related! But maybe..

Abstract
Johne's disease is chronic inflammation of the intestine caused by Mycobacterium avium subspecies paratuberculosis. Infection and disease are mainly in domestic livestock but can affect many species including primates. Johne's is a new disease which emerged at the turn of the 19th and 20th centuries and principally involved Europe and North America. It has since spread to former low incidence regions to become a global problem. Crohn's disease is a chronic inflammation of the intestine in humans which emerged in Europe and North America mid 20th century and increased to become a major healthcare problem. It has now spread to former low incidence regions. Infected animals shed Mycobacterium avium subspecies paratuberculosis in milk and into the environment. Human populations are widely exposed. Outcomes maybe influenced by microbial phenotype. Exposure to extracellular forms of these pathogens may confer some natural protection; exposure to intracellular forms which have passaged through milk macrophages or environmental protists may pose a greater threat to humans particularly individuals with an inherited or acquired susceptibility. Hot spots of human disease such as in Winnipeg which sits on rock at the junction of two rivers may result from local exposure to high levels of waterborne pathogens brought down from farmland. When appropriate methods are used most people with Crohn's disease are found to be infected. There are no data which demonstrate that these pathogens are harmless to humans. An overwhelming balance of probability and Public health risk favours the conclusion that Mycobacterium avium subspecies paratuberculosis is also pathogenic for people. A two tier co-operative pathogenic mechanism is proposed in Crohn's disease. Intracellular infection with the primary pathogen widely distributed throughout the gut causes an immune dysregulation and a specific chronic enteric neuropathy with loss of mucosal integrity. Segments of gross inflammatory disease result from the perturbed neuroimmune response to penetration into the gut wall of secondary pathogens from the lumen. These include both normal gut organisms and educated members of the enteric microbiome such as more aggressive E. coli. More new diseases may arise from failure to apply a range of remedial measures to this longstanding zoonotic problem.

Review
MAP and the emergence of Johne's and Crohn's diseases
Johne's disease (JD) is a systemic infection and chronic inflammation of the intestine in animals caused by Mycobacterium avium subspecies paratuberculosis (MAP). It is most common in ruminants but can affect many other species including primates. It was first seen to emerge in Europe and North America at the end of the 19th and beginning of the 20th centuries. Crohn's disease (CD) in humans is a systemic disorder whose principal clinico-pathological manifestation is also chronic inflammation of the intestine. It is also a new disease which was first seen to emerge in the same continents 40–50 years after JD and increased in frequency steadily until it has become a major healthcare problem. In some areas in the USA in recent years the incidence of CD has seemed to plateau around 7–8 per 105 population per year [1,2]. In Europe the incidence of CD in adults continues to grow [3-5]. Studies in Stockholm, Czech Republic, and Australia supported by data from Finland suggest that the incidence of CD in children in these areas in recent years has been rising in some cases as high as about 5 fold per decade [6-9]. These rapid changes in incidence rule out a primary genetic causation of CD. The data from recent genome wide scans which has identified 32 significant genomic loci related to susceptibility to CD are consistent with the involvement of intracellular bacterial pathogens including mycobacteria, in disease causation [10].

The rising incidence of CD reported from several former low incidence countries in Asia shows that, as with JD, CD is spreading worldwide [11,12]. Recent work from New Zealand reported a high incidence of CD of 16.5 per 105 per year affecting the Canterbury region of South Island with Christchurch as its principal city [13]. Mountains are to the northwest and rivers from them run across rich agricultural pastures and either side of Christchurch before entering the sea. A small river meanders through the city itself. Some of these features are reminiscent of the situation in Cardiff, South Wales UK where a high incidence of CD in city wards bordering the river Taff draining the upland pastures of the Brecons and running through the city was consistent with exposure of the local population to aerosols from the river [14].

A conspicuously anomalous distribution in the incidence of CD exists in North America either side of the Canadian border between Minnesota and Manitoba. In Minnesota to the south the well documented population-based incidence of CD in Olmsted County is 7.9 per 105/year [1] whereas in some areas of the city of Winnipeg little more than 400 miles to the north the incidence reaches a maximum 3.5 fold greater at 28.07 per 105/year [15]. Winnipeg lies astride the junction of the Red River of the North running up from the south and the Assiniboine River coming in from the west. The city sits on bedrock which was once the floor of the immense prehistoric glacial lake Agassiz, with scant run-off in permeable sand and gravel aquifers [16]. The 'hot spot' of CD in the city of Winnipeg we see now is probably due to local exposure of the human population to high levels of waterborne MAP brought down from the agricultural river catchments of the US Midwest, meeting those from the provinces of Manitoba, Saskatchewan and Alberta. Waterborne MAP under these conditions would almost certainly include organisms which have adopted the intracellular phenotype having been taken up by abundant environmental protists [17].

Movement of people and pathogen
Migrant studies show that the incidence of CD in people moving from a low CD and JD incidence area to a high incidence area subsequently rises to that of the host population. The inverse situation is that in which MAP is introduced into an isolated community usually by importation of infected animals. This happened in Iceland in 1933 [reviewed in [18]]. After a latent period following introduction of the pathogen there were at intervals successive epidemics of JD in the island sheep, then in the cattle, then CD in the human population. From 1960 to a peak in 1992 the incidence of CD increased 18 fold. Thus in either case, if people move in amongst MAP or if MAP is moved in amongst people the result is the same namely a steep rise in the incidence of CD. The time interval between the emergence and rise of JD in animals and CD in humans in Iceland was again about 40–50 years. With the almost unlimited opportunity for MAP to spread and evolve in intensively farmed domestic livestock and associated contaminated environments over more than a half century, an evolving virulence and species adaptation of the pathogen would be reflected in the JD to CD interval becoming shorter. A recent example of this happening maybe the steep 4.5 fold increase in CD in the Czech Republic 1995–2007 following the rise in JD caused by the unimpeded importation of subclinically infected cattle from Western Europe after independence in 1990.

Natural Immunity to MAP from environmental and occupational exposure
Why don't dairy farmers and veterinarians exposed to MAP-infected animals get a much higher incidence of CD? Data from the US show that these occupations are in fact associated with a significantly reduced death rate from Inflammatory Bowel Disease [19]. Children exposed to farm animals, particularly cattle, in early life also subsequently have a lower incidence of CD [20]. Occupational exposure to MAP is associated with raised antibody levels to MAP lysates [21]. An answer to the question consistent with these observations is that the extracellular classical ZN-positive phenotype of MAP excreted in trillions by heavily infected animals is not one to which humans are most susceptible. Exposure to this form of the organism may result in the acquisition of some natural immunity to disease. A good example of this happening as a result of purposeful exposure is the approximate 10 fold reduction in clinical Johne's disease achieved subsequently by vaccination of calves using conventional whole killed MAP vaccines with the organisms in this form [22]. The well described urban preponderance of CD may not be that townsfolk have an increased susceptibility to CD, rather that country folk have some natural protection. Passage of MAP through bovine macrophages in milk and cheese or through environmental protists would result in a switch to an intracellular phenotype of MAP likely to have an enhanced virulence for humans [23,24].

MAP and the convergence of candidate pathogens
With the new 21st century, a steadily increasing volume of parallel research has identified three principal sets of bacteria as candidates for the causation of the gross inflammatory disease of the intestine in CD. These are the community of normal gut flora [25], abnormal gut flora such as adherent invasive E. coli (AIEC) [26], and MAP. Because of the global advance of CD and the serious implications for Public Health as well as cumulative individual suffering, there is a need for researchers and clinicians in the field to recognise that the reliable evidence obtained from each of the three lines of inquiry is convergent and that there is actually no conflict between them.

From experimental as well as clinical evidence there is no doubt that bacteria from the normal intestinal microbial community can infect and inflame the gut wall and that they do so in CD. However, the spontaneous emergence and rise of CD in human populations across the globe due to an epidemic of normal gut flora, in the absence of another specific initiating cause, seems rather improbable. The enteric microbiome is a fertile environment for horizontal gene transfer [27]. Advancement of pathogenicity in bacteria may follow the acquisition and mutation of genes and changes in their regulation [28-30]. We already have examples of the pathological consequences of such adaptation in common gut bacteria such as E. coli which can be enteropathogenic, enterohaemorrhagic, enterotoxigenic, enteroaggregative and recently enteroadherent and invasive AIEC [31]. Such adaptations usually arise due to the imposition of some external selection pressure. Recent evidence also suggests that common enteric bacteria like E. coli may display predictive behaviour [32].

The principal property of MAP which distinguishes it from all other candidate pathogens in the primary causation of CD is that it is an established multi-host chronic enteric pathogen. MAP has the proven specific ability to initiate and maintain chronic inflammation of the intestine of a range of different histopathological types in many species including primates. MAP infection in animals causes a local and systemic immune dysregulation. It is also specifically neuropathogenic especially for non-myelinated neurones and intestinal disease is accompanied by a chronic enteric neuropathy [33]. Despite its broad pathogenicity, MAP infection can persist in animals for years without necessarily progressing to clinical disease. Clinical disease in animals when it occurs is commonly of the pluribacillary type but paucimicrobial disease with the pathogens in a Ziehl Neelsen (ZN)-negative phenotype is well described.

The overall prevalence of MAP infection in US dairy herds is reported by a USDA survey to be 68.1% [34]. A range of broadly similar data shows that MAP infection in farm animals is widespread in many areas of Western Europe and elsewhere. MAP contaminates and persists in water and the environment, is in dairy products, can survive milk pasteurisation, and is present in meat from infected animals. It is inevitable that human populations are widely exposed.

MAP in humans
MAP infection in humans is difficult to detect. The organisms are present in low abundance in a robust ZN-negative phenotype. They are intracellular and minimise their own immune recognition. They are extremely difficult to isolate and propagate in culture and are relatively resistant to chemical and enzymatic lysis. Reliable access to their DNA is only achieved during sample processing by combining exposure to stringent lysis buffers with an additional optimised mechanical disruption step. Freezing samples and tissue extracts especially at -20°C substantially reduces the PCR detection rate of their GC-rich DNA. The organisms have been cultured and detected in blood showing that, as in animals, the infection in humans is systemic [35-37]. At present, the benchmark diagnostic test for MAP infection in humans is nested PCR applied to single ~20 mg fresh endoscopic mucosal biopsies [38]. When validated methodologies have been used most people with CD have been found to be infected with MAP [39]. In simple words, most people with chronic inflammation of the intestine (of the CD type) are infected with a mycobacterium which is a proven specific cause of chronic inflammation of the intestine. There are no data which demonstrate that MAP are harmless to humans. The overwhelming balance of probability and public health risk favours the conclusion that MAP are also pathogenic for people.

Inflammation in Crohn's disease caused by a two tier co-operative pathogenic mechanism
MAP infects the gut widely in CD and is found both in the more normal looking intestine and the grossly inflamed and diseased segments of intestine [33]. MAP antigens have appeared to dominate the immunological responses of intestinal CD4 T cell lines from patients with CD [40]. Mannans released by MAP inhibit intracellular killing of internalised bacteria [41].

The MAP infection causes a primary microscopic inflammation accompanied by a specific immune dysregulation and enteric neuropathy [33]. Mucosal integrity and other critical functions of the intestine are impaired. The visible segments of gross inflammatory disease result from the perturbed neuroimmune response to the secondary penetration into the gut wall of gut flora containing both normal intestinal bacteria and those which have undergone transformations leading to a more invasive phenotype like AIEC. It is important to note that genomic loci in the host conferring genetic susceptibility to Crohn's disease have the potential to operate at the levels of both primary and secondary pathogens. The entry of food residues into the gut wall contributes an allergic component to the inflammatory mess. Although MAP has been found in intestinal granulomas in humans [42], the presence or absence of these and other features of the variable histopathological picture of CD are principally determined by the large scale response to the secondary co-pathogens including especially other granulomatous species like M. avium subspecies avium which are frequently recovered in culture from CD tissues [38]. Thus the three lines of contemporary research inquiry come together in a two tiered co-operative pathogenic mechanism.

MAP doomsday
Imagine the collective human enteric microbiome in, say, a crowded Europe. A vast composite structure made up of millions of individual highly mobile microbial reservoirs variably interconnected in time and space and degree. A dynamic structure possessing an inherent self governing order and stability not easily displaced. Into this cellular system is progressively introduced a slowly growing specific mycobacterial pathogen which has acquired the genetic machinery necessary to cloak itself with a predicted fucosylated surface [43] so that it conforms with the familiar molecular environment particularly of the host's epithelial cells and mucosal compartment [44]. It has come from the parallel universe of the collective enteric microbiome of human food animals and before that from the soil. It causes a microscopic inflammation and perturbs the microenvironment of the mucosa and gut wall. To survive and prosper it minimises its confrontation with the human immune system. It causes a variable immune dysregulation but it also inflames the fine structure and function of the enteric nervous system.

More than a hundred years go by. Both animal and human total microbiomes swell with increasing population density. The mycobacterial pathogen acquires additional properties resulting in an evolution in its behaviour with an increase in pathogenicity and species range. Some normal inhabitants of the enteric microbiome adapt to the disturbed intestinal microenvironment and they too acquire characteristics which make them more invasive. Chronic enteric disease emerges and spreads particularly in individuals with an inherited or acquired susceptibility. Humans responsible for controlling and managing these diseases, blind to what is really happening are distracted by detail and dismissive. The required remedial measures are not designed and applied and the problems get worse. Left undisturbed, maybe the education in hostility already received by increasingly aggressive members of the former normal gut flora will progress to the point where they too can emerge from background to become primary independent pathogens in their own right. When they do so more new diseases will emerge.

Can anti-MAP treatment heal Crohn's disease?
The answer to this question supported by a correct interpretation of data both from open label studies [45-48] and the Australian controlled clinical trial is a qualified yes [49-51]. It can in some people with CD some of the time. When it does so in 'responders' receiving treatment with drug combinations including rifabutin and clarithromycin the clinical and pathological improvement can be dramatic and has been associated with the conversion of pre-treatment MAP positive tests in blood [52] and gut mucosa (my own unpublished observations) to negative. Furthermore, some of the clinical benefit resulting from treatment of CD with conventional 'immunosuppressive' agents such as 6-mercaptopurine or methotrexate may actually be a consequence of their demonstrable direct anti-MAP action [53-55]. But MAP infections are difficult to eradicate. The organisms are generally resistant in vivo to drugs conventionally used in the treatment of tuberculosis. Treatment is prone to all the problems of microbial drug resistance and latency encountered in the management of chronic lung disease caused by other members of the M. Avium Complex.

New clinical trials are needed of anti-MAP treatment in CD particularly of agents developed for the treatment of M. tuberculosis which are active against mycobacteria in the non-replicative state [56] and where the gene encoding the molecular target is shared by MAP. Rich clinical and commercial rewards are out there for those who do so successfully.

Conclusion
Recognition and acceptance of the true nature of the expanding long term threat to human health posed by widespread exposure to MAP, based upon a perceptive understanding of the problem and the overwhelming balance of reliable scientific evidence, is a matter of urgency. The solutions lie in the identification and incremental introduction of a range of remedial measures which are both scientific and regulatory whose effective application on a global scale requires close international cooperation.

I just finished watching those videos too. Aside from everything else, the bit that stood out to me the most was when he was talking about it being airborne (in either the 2nd or third part, Ican't remember) and people breathing it in and developing a cough before they developed Crohn's. That's exactly what happened to me. I had this horrible persistent cough for a couple of weeks before my Crohn's symptoms started showing up. Until that video I never would have thoughts the two would be related! But maybe..

my son dx @ 10 yrs old had (and still has) a persistent cough for about 4 years or so doctors can only say its post nasal drip

Im with you, I've definitely started celebrating far too soon but i couldnt sleep last night after watching those youtube videos of his speech. The government needs to give this man some damn money so he can do his trials already!

...and if it turns out not to work ill start trying fecal transplants.

...and if that doesnt work i'll call it a day, move to amsterdam, and get high until i run out of money.

The money is the least of all problems, if that is the only thing being left for the vaccine to become a reality, then we´ll start a petition/crowdsourcing.

I will contact them as soon as they open again.

let us know how you go w contacting them please. i'm hopefully going to be starting anti-map therapy in feb. praying it is the thing that fixes me up. upon lots of research I am very hopeful but as we all know w this disease theres such an element of unknown that hangs over us like a dark shadow.

Joshua - good luck with the anti-map; hopefully it will get you into deep steady remission. How are you going to do this ? do you have a DR who will treat you bythis protocol ? are you participating in some trial ?

Hi worriedboy, I'm going to see dr Borody who will do a scope on me and then pending tests start me on the therapy. Thanks for the well wishes, I do believe it's going to be the thing that works. By process of elimination the only thing that could be causing my illness is an infection, if it were my immune system going haywire then the immuno suppressants would be working...

MAP doesn't cause all cases, crohns likely has multiple causes, I don't think there is any disease that is just caused by one particular pathogen/bacteria. But hopefully this will be a cure for the vast majority of people with crohns. AEIC is another potential causative. Theres a lot of unknowns but one thing is for certain, crohns certainly is not an auto-immune disease, it's an infection, they're finding out now that the reason remicade may have the success it does
Is because it kills cells that are infected.

I'd like to add that Koch's postulates (the scientific criteria required to prove something causes a disease) has been fulfilled for MAP and crohn's, so that's not open for discussion, it's like trying to argue gravity. What's frustrating is so many practitioners aren't even aware of Koch's postulates... Furthermore, in an early anti-map trial (I posted the results on the forum somewhere) anti-map has had the highest remission rate ever reported, and that was a flawed design that actually made the results appear less effective, the remission response was 66% at 16+ weeks I believe, remicade was 36% at 26 weeks, ad they used CDAI which is notoriously unreliable.

To the people who think large drugs companies are going to try to ban this vaccine - you can't think that way about all of these cures/vaccines that exist. Drug companies will profit from such vaccines by manufacturing/distributing them. Think about it - there are loads of vaccines available for a variety of diseases that could otherwise be 'treated' temporarily.

Everybody needs to go on that "run for Crohns" page on facebook, on that page is alink to a charity set up by Amy Herman Taylor, the professors daughter.

Sadly we're not allowed to promote charity collections on the forum for some reason. It would be nice to be able to get the word out to a large group of crohns sufferers so that some worthwhile donations could be made. I can't see why anybody with crohns wouldn't be willing to at least throw a tenner their way, even if they dont believe the MAP idea.